lumpy skin disease
- Host Animals
- Hosts/Species Affected
- Systems Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Links to Websites
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- lumpy skin disease
International Common Names
- English: lumpy skin disease, capripoxvirus, in cattle- exotic; yak pox
- French: dermatose nodulaire contagieuse; la dermatose nodulaire contagieuse
OverviewTop of page
A disease was first described in Northern Rhodesia (Zambia) in 1929, which was initially thought to be due to an allergic reaction in cattle to biting insects (MacDonald, 1931). This was because it appeared usually at that time of year when populations of biting insects were at their greatest. It recurred fairly frequently there, and in 1943 the same syndrome was described in Botswana (von Backstrom, 1945). This raised further questions about its aetiology, and then in 1945 it was reported in Southern Rhodesia (Zimbabwe), Mozambique, and in South Africa (Huston, 1945). Whether these new foci of disease were the result of spread from the original foci in Zambia or whether it had hitherto not been recognised in these two countries is not clear. The suggestion is that lumpy skin disease (LSD) spread from the original foci in Zambia.
This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's WAHID Interface database on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. Also see the website: www.oie.int
Host AnimalsTop of page
Hosts/Species AffectedTop of page
Natural infections with LSD have only been described in cattle in sub-Saharan Africa, and both Bos taurus and Bos indicus breeds, are susceptible. Bos taurus animals exotic to Africa are generally more susceptible than the zebu-type cattle, which are indigenous to sub-Saharan Africa. A single clinical case of a Capripox infection, probably LSD, was described in an Arabian oryx in a zoo in Saudi Arabia. Many wild ruminant species, which share grasslands with cattle in many parts of Africa, are not naturally infected with LSD as a clinical syndrome. These have been carefully surveyed in areas where active LSD virus transmission was taking place, but no LSD lesions could be seen in wild buffalo (Syncerus caffer), impala (Aepyceros melampus), waterbuck (Kobus defassa), or the gazelle species. However, wild animals showing severe clinical signs of LSD are likely to be eliminated by predators which could explain the lack of reports of clinical disease in wildlife species. Also the presence of clinical signs of LSD in wildlife is easily missed as the monitoring of the skin lesions is difficult or impossible, especially in mild cases. Serum antibody to Capripox viruses was however found in buffalo populations from areas contiguous with those where LSD transmission was actively taking place, and not in those far distant from any LSD foci (Davies, 1982; Barnard, 1997). Subsequently, antibody to Capripox has been found in other game animals, which suggests that several species may be subclinically infected with LSD. However, this antibody may have been produced by a Capripox strain other than LSD (Davies.1982; Hamblin et al., 1990).
No obvious clinical LSD was evident in Asiatic buffalo herds (Bubalis bubalis) held in close contact with infected cattle during the Egyptian LSD epidemic; many thousands of animals were inspected during the epidemic. A report of 5 clinical cases based upon histopathological examination was not supported by virus isolation. Experimental studies in Egypt showed that the buffalo was refractory to needle inoculation with LSD virus, and no lesions developed.
The first LSD outbreak in Kenya was at a farm where there was a concurrent outbreak of sheep pox (Burdin, 1959). The possibility was raised that there may have been a change in the host affinity of the virus and that it may have crossed from sheep and goats to infect the cattle. Certainly, the lesions of LSD and of KSGP are identical in the different species, and the viruses are the same in all characteristics. This has recently been confirmed by DNA fingerprinting of the Kenya sheep and goat pox and LSD viruses (Black et al., 1986; Gershon and Black, 1988). They are indistinguishable by most laboratory test systems. The possibility that cross infection may have occurred cannot be denied. However it must be noted that for 40 years, LSD has occurred in cattle held in close contact with sheep and goats, and sheep and goat pox has occurred in these animals held together with cattle. No cross infection has ever been encountered or manifested by the development of lesions or sero-conversions in the other species. In South Africa where LSD occurs in cattle and where there are 40 million sheep, sheep and goat pox does not exist.
Sheep and goats develop LSD-like lesions, when inoculated intra-dermally with LSD virus, and cattle likewise develop a similar lesion when inoculated with KSGP virus (Capstick, 1961). Some mild generalised lesions can develop in Bos indicus cattle inoculated with the KSGPV vaccines which are used to protect sheep and goats against this disease, and these can be more serious in highly susceptible Bos taurus breeds. Such strains are highly modified for sheep and goats, however where they are potent immunogens.
Camels are not normally affected by LSD. A single natural clinical case of LSD was found in an Arabian oryx in Saudi Arabian zoo (Greth et al., 1992). Experimental inoculation of impala (Aepyceros melampus), of Thomsons gazelle (Gazella thomsonii) and the giraffe (Giraffa camelopardalis) was followed by the development of LSD lesions in the skin (Young et al., 1968). Such lesions have not been observed during the LSD epizootics in Africa. Recently, the persistence of LSDV nucleic acid was reported in skin samples collected from springbok (Antidorcas marsupialis) in South Africa (Lamien et al., 2011).
Laboratory animals such as rabbits, guinea pigs and mice are refractory to infection with LSD. The virus replicates in embryonated hens eggs, when inoculated by the chorio- allantoic route. The virus grows and adapts slowly to produce some oedema of the membrane and low virus titres, which increase with adaptation and may produce small pocks after 5-6 passages at 34.5°C (van Rooyen et al., 1968).
Systems AffectedTop of page digestive diseases of large ruminants
multisystemic diseases of large ruminants
respiratory diseases of large ruminants
skin and ocular diseases of large ruminants
DistributionTop of page
LSD is thought to have originated in Zambia from where it spread to Zimbabwe, Mozambique, and South Africa. The transmissible character of LSD quickly became apparent after its spread to South Africa, when it assumed epizootic proportions and in 2-3 years extended over most of the country. More than 8 million cattle were affected in the outbreak and the economic losses sustained were considerable. The losses resulted directly from mortality, which occurs in many young and some older animals and from the loss in production, which results from debility caused by the disease, particularly the extensive skin lesions, which restrict mobility (Diesel, 1949). A further and most significant effect is the damage to hides, caused by the full skin thickness lesions, which render hides useless or at best, resulting in a very poor grading (Green, 1959).
In 1957, LSD was first seen in East Africa in Kenya in the Rift Valley, in a fairly localised outbreak (Burdin, 1959). Subsequently, epidemics of LSD have occurred irregularly and have extended to include the whole of Kenya, and have also been reported from Uganda, Somalia and Tanzania. The disease was reported from the Nile basin of southern Sudan in the early 1970s (Ali and Obeid, 1977) and then in the period 1970-1990 it occurred in most of the central and West African countries (Nawathe et al., 1978), where it has persisted and recurs at irregular intervals ever since (Khallafalla et al., 1993). LSD was also reported from Madagascar. It may today be said to be endemic in most African countries.
In 1988, foci of LSD were reported for the first time from Egypt, where it had a dramatic impact upon intensive milk-producing herds (Ali et al., 1990). These herds were made up of imported Friesian /Holstein breeds which are highly susceptible to LSD; the disease had a serious effect upon milk production and supplies. The initial focus of infection was seen in Ismailyia, not far from a quarantine centre, and extended from Aswan to the desert oasis, affecting 22 of 26 'governates' of the country by the summer of 1989. A limited focus of disease was also detected in Israel 80 km away, and was initially eradicated from the country by a slaughter policy, although it has subsequently returned (Yeruham et al.,1995). At approximately the same time, LSD was reported from the countries of the Arabian peninsula (Greth et al., 1992). After an apparent absence of 17 years, LSD re-occurred in Egypt in 2006, being introduced into the country by infected cattle imported from the African Horn countries (El-Kholy et al., 2008). In June 2006 cases of LSD were again reported in Israel (Brenner et al., 2009). According to the OIE LSD has been reported in Kuwait in 1991, Lebanon in 1993, Yemen in 1995, United Arab Emirates in 2000, Bahrain in 2003, Israel in 2006-7, and Oman in 2010 (Shimshony and Economides, 2006).
There is considerable risk of further spread of LSD in the Middle East. Countries at the greatest risk are thought to be Syria, Lebanon and Turkey in the Eastern Mediterranean, and Iran and Iraq, which have highly vulnerable areas for LSD outbreaks with abundant potential insect vectors. LSD may be considered to be an emerging animal disease of some importance at a time when global warming is altering the microclimate of some regions in favour of arthropod vectors. Once LSD has occurred in a country, it has proved virtually impossible to eradicate.
All the available evidence confirms the field observations that epidemics of LSD occur at periods of greatest biting insect activity. However, attack rates in different epidemics have varied from 10-15% to nearly 100%, and it may be that different vector species are active in different situations. Lower levels of transmission occur in dry conditions, where the common biting flies such as Stomoxys, tabanids and tsetse flies are likely to be implicated. Very high morbidity rates occur only when mosquito-breeding sites are extensive and insect populations are high after rain. The mechanisms of the transmission of LSD have not been fully clarified (Weiss, 1968; Kitching and Mellor, 1986; Carn and Kitching, 1995). Recently, new evidence has been published reporting a possible role for hard ticks in the transmission of LSDV (Tuppurainen et al., 2011). The study showed molecular evidence of transstadial and transovarial transmission of LSDV by Rhipicephalus (Boophilus) decoloratus ticks, and mechanical or intrastadial transmission by Rhipicephalus appendiculatus and Amblyomma hebraeum ticks.
During 2011, 26 African countries reported outbreaks of LSD to AU-IBAR. A total of 902 epidemiological units were affected by the disease, involving 33,750 cases and 1,305 deaths. The highest number of cases were reported from DRC (7,551), followed by Ethiopia (6,226), Uganda (5,824), Burkina Faso (4,013), and Madagascar (3,767) in 2011 (AU-IBAR, 2011). Given the mode of transmission of LSD, the low figures for outbreaks as reported by Cameroon, Gambia, Mali, Niger, Senegal and Somalia may reflect under-reporting.
Countries reporting LSD to AU-IBAR in 2011:
Although LSD seems to have occurred throughout the year, relatively higher number of outbreaks were reported from the cooler periods of November, December, January, February and March, which may be attributed to a higher abundance of vectors during that period in the severly affected countries.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Afghanistan||No information available||OIE, 2009|
|Armenia||Disease not reported||OIE, 2009|
|Azerbaijan||Disease never reported||OIE, 2009|
|Bahrain||Absent, reported but not confirmed||OIE, 2009|
|Bangladesh||Disease never reported||OIE, 2009|
|Bhutan||Disease never reported||OIE, 2009|
|Brunei Darussalam||Disease not reported||OIE Handistatus, 2005|
|Cambodia||No information available||OIE, 2009|
|China||Disease never reported||OIE, 2009|
|-Hong Kong||No information available||OIE, 2009|
|Georgia (Republic of)||Disease not reported||OIE Handistatus, 2005|
|India||Disease never reported||OIE, 2009|
|Indonesia||Disease never reported||OIE, 2009|
|Iran||Disease never reported||OIE, 2009|
|Iraq||Disease never reported||OIE, 2009|
|Israel||Disease not reported||200711||Yeruham et al., 1994; Yeruham et al., 1995; OIE, 2009|
|Japan||Disease never reported||OIE, 2009|
|Jordan||Disease never reported||OIE, 2009|
|Kazakhstan||Disease not reported||OIE, 2009|
|Korea, DPR||Disease not reported||OIE Handistatus, 2005|
|Korea, Republic of||Disease never reported||OIE, 2009|
|Kuwait||Disease not reported||OIE, 2009|
|Kyrgyzstan||Disease never reported||OIE, 2009|
|Laos||Disease not reported||OIE, 2009|
|Lebanon||Disease not reported||OIE, 2009|
|Malaysia||Disease never reported||OIE, 2009|
|-Peninsular Malaysia||Disease never reported||OIE Handistatus, 2005|
|-Sabah||Disease never reported||OIE Handistatus, 2005|
|-Sarawak||Disease never reported||OIE Handistatus, 2005|
|Mongolia||No information available||OIE, 2009|
|Myanmar||Disease never reported||OIE, 2009|
|Nepal||No information available||OIE, 2009|
|Oman||No information available||OIE, 2009|
|Pakistan||Disease never reported||OIE, 2009|
|Philippines||Disease never reported||OIE, 2009|
|Qatar||No information available||OIE, 2009|
|Saudi Arabia||Disease never reported||OIE, 2009|
|Singapore||Disease never reported||OIE, 2009|
|Sri Lanka||Disease never reported||OIE, 2009|
|Syria||Disease not reported||OIE, 2009|
|Taiwan||Disease never reported||OIE Handistatus, 2005|
|Tajikistan||Disease never reported||OIE, 2009|
|Thailand||No information available||OIE, 2009|
|Turkey||Disease never reported||OIE, 2009|
|Turkmenistan||Disease never reported||OIE Handistatus, 2005|
|United Arab Emirates||Disease not reported||OIE, 2009|
|Uzbekistan||Disease never reported||OIE Handistatus, 2005|
|Yemen||No information available||OIE, 2009|
|Algeria||Disease never reported||OIE, 2012|
|Botswana||Present||von Backstrom, 1945; OIE, 2012|
|Burkina Faso||Present||OIE, 2012|
|Burundi||Reported present or known to be present||OIE Handistatus, 2005|
|Cameroon||Last reported||2011||OIE, 2012|
|Cape Verde||Disease never reported||OIE, 2012|
|Central African Republic||Disease not reported||OIE, 2012|
|Chad||No information available||OIE, 2009|
|Congo||No information available||OIE, 2009|
|Congo Democratic Republic||Present||AU-IBAR, 2011|
|Côte d'Ivoire||Last reported||2001||OIE Handistatus, 2005|
|Djibouti||Disease not reported||OIE, 2009|
|Egypt||Last reported||2006||Ayre-Smith, 1960; Ali et al., 1990; House et al., 1990; Michael et al., 1997; OIE, 2012|
|Gabon||Disease never reported||OIE, 2012|
|Kenya||Last reported||2007||Burdin, 1959; MacOwan, 1959; Black et al., 1986; Gershon and Black, 1988; OIE, 2012|
|Libya||Disease never reported||OIE, 2012|
|Mauritius||Last reported||2008||OIE, 2012|
|Morocco||Disease never reported||OIE, 2012|
|Mozambique||Present||Huston, 1945; OIE, 2012|
|Niger||Restricted distribution||OIE, 2012|
|Nigeria||Present||Nawathe et al., 1982; OIE, 2012|
|Réunion||Disease not reported||OIE Handistatus, 2005|
|Sao Tome and Principe||Disease not reported||OIE Handistatus, 2005|
|Seychelles||Disease not reported||OIE, 2012|
|Somalia||Nawathe et al., 1982; OIE, 2012|
|South Africa||Present||Huston, 1945; Diesel, 1949; OIE, 2012|
|Sudan||Present||Ali and Obeid, 1977; Khalafalla et al., 1993; OIE, 2012|
|Tanzania||Present||Nawathe et al., 1982; Hamblin et al., 1990; OIE, 2012|
|Tunisia||Disease never reported||OIE, 2009|
|Uganda||Present||Nawathe et al., 1982; OIE, 2012|
|Zambia||Present||MacDonald, 1931; OIE, 2012|
|Zimbabwe||Present||Huston, 1945; OIE, 2012|
|Bermuda||Disease not reported||OIE Handistatus, 2005|
|Canada||Disease never reported||OIE, 2009|
|Greenland||Disease never reported||OIE, 2009|
|Mexico||Disease never reported||OIE, 2009|
|USA||Disease never reported||OIE, 2009|
Central America and Caribbean
|Barbados||Disease never reported||OIE Handistatus, 2005|
|Belize||Disease never reported||OIE, 2009|
|British Virgin Islands||Disease never reported||OIE Handistatus, 2005|
|Cayman Islands||Disease never reported||OIE Handistatus, 2005|
|Costa Rica||Disease never reported||OIE, 2009|
|Cuba||Disease never reported||OIE, 2009|
|Curaçao||Disease not reported||OIE Handistatus, 2005|
|Dominica||Disease not reported||OIE Handistatus, 2005|
|Dominican Republic||Disease never reported||OIE, 2009|
|El Salvador||Disease never reported||OIE, 2009|
|Guadeloupe||Disease never reported||OIE, 2009|
|Guatemala||Disease never reported||OIE, 2009|
|Haiti||Disease never reported||OIE, 2009|
|Honduras||Disease never reported||OIE, 2009|
|Jamaica||Disease never reported||OIE, 2009|
|Martinique||Disease never reported||OIE, 2009|
|Nicaragua||Disease never reported||OIE, 2009|
|Panama||Disease never reported||OIE, 2009|
|Saint Kitts and Nevis||Disease never reported||OIE Handistatus, 2005|
|Saint Vincent and the Grenadines||Disease never reported||OIE Handistatus, 2005|
|Trinidad and Tobago||Disease never reported||OIE Handistatus, 2005|
|Argentina||Disease never reported||OIE, 2009|
|Bolivia||Disease never reported||OIE, 2009|
|Brazil||Disease never reported||OIE, 2009|
|Chile||Disease never reported||OIE, 2009|
|Colombia||Disease never reported||OIE, 2009|
|Ecuador||Disease never reported||OIE, 2009|
|Falkland Islands||Disease never reported||OIE Handistatus, 2005|
|French Guiana||Disease not reported||OIE, 2009|
|Guyana||Disease never reported||OIE Handistatus, 2005|
|Paraguay||Disease never reported||OIE Handistatus, 2005|
|Peru||Disease never reported||OIE, 2009|
|Uruguay||Disease never reported||OIE, 2009|
|Venezuela||Disease never reported||OIE, 2009|
|Andorra||Disease never reported||OIE Handistatus, 2005|
|Austria||Disease never reported||OIE, 2009|
|Belarus||Disease never reported||OIE, 2009|
|Belgium||Disease never reported||OIE, 2009|
|Bosnia-Hercegovina||Disease never reported||OIE Handistatus, 2005|
|Bulgaria||Disease never reported||OIE, 2009|
|Croatia||Disease never reported||OIE, 2009|
|Cyprus||Disease never reported||OIE, 2009|
|Czech Republic||Disease never reported||OIE, 2009|
|Denmark||Disease never reported||OIE, 2009|
|Estonia||Disease never reported||OIE, 2009|
|Finland||Disease never reported||OIE, 2009|
|France||Disease never reported||OIE, 2009|
|Germany||Disease never reported||OIE, 2009|
|Greece||Disease never reported||OIE, 2009|
|Hungary||Disease never reported||OIE, 2009|
|Iceland||Disease never reported||OIE, 2009|
|Ireland||Disease never reported||OIE, 2009|
|Isle of Man (UK)||Disease never reported||OIE Handistatus, 2005|
|Italy||Disease never reported||OIE, 2009|
|Jersey||Disease never reported||OIE Handistatus, 2005|
|Latvia||Disease never reported||OIE, 2009|
|Liechtenstein||Disease not reported||OIE, 2009|
|Lithuania||Disease never reported||OIE, 2009|
|Luxembourg||Disease never reported||OIE, 2009|
|Macedonia||Disease never reported||OIE, 2009|
|Malta||Disease never reported||OIE, 2009|
|Moldova||Disease never reported||OIE Handistatus, 2005|
|Montenegro||Disease never reported||OIE, 2009|
|Netherlands||Disease never reported||OIE, 2009|
|Norway||Disease never reported||OIE, 2009|
|Poland||Disease never reported||OIE, 2009|
|Portugal||Disease never reported||OIE, 2009|
|Romania||Disease never reported||OIE, 2009|
|Russian Federation||Disease never reported||OIE, 2009|
|Serbia||Disease never reported||OIE, 2009|
|Slovakia||Disease never reported||OIE, 2009|
|Slovenia||Disease never reported||OIE, 2009|
|Spain||Disease never reported||OIE, 2009|
|Sweden||Disease never reported||OIE, 2009|
|Switzerland||Disease never reported||OIE, 2009|
|UK||Disease never reported||OIE, 2009|
|-Northern Ireland||Disease never reported||OIE Handistatus, 2005|
|Ukraine||Disease never reported||OIE, 2009|
|Yugoslavia (former)||Disease never reported||OIE Handistatus, 2005|
|Yugoslavia (Serbia and Montenegro)||Disease never reported||OIE Handistatus, 2005|
|Australia||Disease never reported||OIE, 2009|
|French Polynesia||Disease never reported||OIE, 2009|
|New Caledonia||Disease never reported||OIE, 2009|
|New Zealand||Disease never reported||OIE, 2009|
|Samoa||Disease never reported||OIE Handistatus, 2005|
|Vanuatu||Disease never reported||OIE Handistatus, 2005|
|Wallis and Futuna Islands||No information available||OIE Handistatus, 2005|
PathologyTop of page
The removal of the skin of LSD affected animals shows extensive yellow-red tinged oedematous fluid in the subcutis, associated with lesions. There may be a local cellulitis associated with some lesions and the regional lymph nodes are grossly enlarged and may have pyaemic foci. The nodular LSD lesions may be visible in the fascia over limb muscle and often in muscle tissue itself. On section, the lesions are grey-white surrounded by red inflammatory tissue. The characteristics of the nodules are basically the same, whether they are found throughout the carcass, in the kidney, they are usually 10-30 mm diameter. The lungs may have many scattered small 10-20 mm lesions which look like secondary carcinoma, they are due to an infiltration with the large epithelioid 'celles claveleuses', described by Borrel for sheep pox. An interstitial or bronchopneumonia may be associated with these lesions if they are widespread. Alimentary lesions are commonest in the abomasum, where necrotic tissue forms an ulcer. Lesions are not normally seen on the serosal surfaces of the body cavities, nor in the liver, cardiovascular nor nervous systems.
The lesions in the nasal mucosa and the oropharynx have the characteristic ring appearance peculiar to LSD, due to the separation of the necrotic epithelium away from the healthy tissue surrounding the lesion. Such lesions may be seen on the muzzle, nares and larynx, on the gingiva and hard and soft palate. They may also be seen in the trachea and bronchi. The necrotic tissue sloughs away to leave an ulcer that slowly heals by granulation. Regional lymph nodes will be enlarged and oedematous, and can be 3-5 times their usual size.
The histo-pathological changes, which can be seen in skin sections from LSD cases are characteristic of the disease, and provide a basis for diagnosis. There is an oedema and infiltration of the epidermis and dermis with large epithelioid macrophage type cells, which have also been well described for sheep pox. They are found with plasma cells and lymphocytes in early lesions, and in older lesions, fibroblasts and polymorphonuclear leucocytes with some red cells predominate. Endothelial proliferation is seen in the blood vessels of the dermis and subcutis, with lymphocytic cuffing of the blood vessels. The thrombosis and necrosis results from this. Specific intra-cytoplasmic inclusions may be found in the various epithelial elements, sebaceous glands and follicular epithelium. These are largely eosinophilic-purple and appear to have a clear halo surrounding them, which is probably a processing artefact. The lesions are substantially the same throughout the body (Burdin, 1959).
DiagnosisTop of page
The diagnosis of LSD may be tentatively made after appearance of the typical skin lesions. Rapid and accurate laboratory confirmation of the diagnosis enables the swift implementation of appropriate measures to control the spread of the disease.
Sample collection: Skin biopsies should be taken from at least 3 affected animals at an early stage of lesion development before they become hard. Elliptical sections are cut aseptically under local anaesthetic from shaved areas around an early lesion. Alternatively, lesion material can be collected from lesions in muscle or other tissue at postmortem. Biopsy material is held in a transport medium (such as 20-50 % glycerol in phosphate buffered saline) containing antibiotics. The skin biopsy should contain skin lesion with a small area of normal skin. A second sample is collected in formal saline or kept on ice for cryostat sectioning. This material can be used for all of the diagnostic methods. EDTA blood should be collected for PCR and heparin blood for virus isolation.
Identification of live virus or antigen
The use of cell cultures has replaced the use of live animals in the diagnostics of LSDV. However, if required and in case, high containment isolation animal facilities are available, thin-skinned susceptible calves can be inoculated by intradermal route with dilutions of the virus. Intradermal inoculation of a calf may be made with 0.1 ml aliquots of a 10% homogenate of the biopsy in a transport medium. This should be diluted further to 1/100 to 1/100,000, and inoculated at 4 sites per dilution on the shaved side of the calf. The lesions will appear after 5-9 days and show the characteristic form of LSD skin reaction. Further biopsy material can then be taken.
Agar gel precipitation
The large pox viruses share antigens with some of the other pox viruses including parapox, and this test is not specific for LSD.
Skin biopsy material may be sectioned either from formal saline fixed material or in a cryostat. Simple Haematoxylin and Eosin (H and E) staining will show the distinctive features of LSD lesions: full skin thickness cellular infiltration, intracytoplasmic inclusions, and thrombosis of the blood vessels with necrosis. The method serves to distinguish LSD from streptothricosis, globidiosis (besnoitiosis), allergic skin reactions, and bovine herpes type 2 infections with which it can be confused.
If available, this provides a rapid means for the diagnosis of LSD. The method should be used with at least three different sets of biopsy material from different affected animals. This is due to the possible misdiagnosis, often made, when orphan or other herpes viruses are seen in large numbers in the lesion material.
Simple negative staining with phosphotungstic acid may be carried out. Taking a needle, insert it into the lesion material and wash this into a drop of distilled water. A 400 mesh carbon-coated grid is then placed on the drop, blotted and stained with PTA in 0.4 % glucose at pH 7.0 for 1 min. Prepare several grids from each sample and examine at 6000-18,000 magnification. The large brick-shaped Capripox virus particles are readily seen in most lesion material (Davies et al., 1971).
Lumpy skin disease virus can be cultured in a large variety of tissue cultures. Pre-pubertal lamb or bovine testis cultures or bovine dermis cells at primary or secondary level are the most sensitive system. Lamb or calf kidney cells are generally of log 10 lower in sensitivity than those of testicular origin, as are many ovine or bovine foetal tissues including skin, muscle, lung, endothelial or thyroid cells. The cell lines of bovine or sheep kidney cells, rabbit kidney, Vero and others have been used in laboratories for work on LSD but they are not as sensitive as testis cultures for primary isolation (Alexander et al., 1957; Plowright and Witcomb, 1959). There may, however, be some differences in the sensitivity of testicular tissues derived from different breeds and strains of sheep. Recently, commercially available lamb testis cell line (OA3.Ts) has been evaluated for propagation of capripoxvirus isolates (Babiuk et al, 2007). The biopsy material should be minced with scissors and ground in a pestle with sterile sand, with approximately 2-3 times the w/v of transport medium. In order to release the intracellular virus, samples can be either sonicated twice for 15 seconds or the slurry can be frozen and thawed three times, and made up to a 5-10% suspension in the transport medium. This is centrifuged to remove the debris at 800 g for 10 min. Especially, when virus is isolated from skin samples, in order to reduce the bacterial contamination in cell culture, supernatant is filtered through 0.45 µm pore size filter before it is inoculated into a tissue culture flask, tube or slide well cultures, which have 75-80 % cell cover. It is then desirable to inoculate coverslip preparations or slide well cultures for antigen detection after 48-72 h. LSD viral antigen may be seen in positive cultures fixed and stained by immunofluorescent, immunoperoxidase or H and E staining methods as round spherical bodies of antigen in the cytoplasm (intracytoplasmic inclusion bodies). The cytopathic effects (CPE) produced by the virus appear after 4-10 days as foci of increased density in cells, which round up and strand across gaps in the monolayer. Such areas gradually enlarge to include most of the monolayer (Plowright and Witcomb, 1959; Davies et al., 1971). Negative cell cultures should be blind passaged after 14 days as a routine procedure.
ELISA antigen capture
This will be a valuable diagnostic tool should it become more readily available in kit form. A Capripox polyclonal antibody is used in a capture test system and this compares well with virus isolation in tissue culture. Like most ELISA capture methods, it is however 2-3 log 10 TCID 50 less sensitive than tissue cultures for primary isolation. However, the test is highly specific and has the advantage that it does not depend upon sophisticated laboratory facilities. It should become the diagnostic tool of choice in many laboratories in countries where LSD is enzootic (Fick and Viljoen, 1999; Ngichabe et al., 1999).
Polymerase chain reaction (PCR)
Several conventional PCR (Heine et al., 1999; Ireland and Binepal, 1998; Mangana-Vougiouka et al., 1999; Orlova et al., 2006; Tuppurainen et al., 2005; Zheng et al., 2007) and real-time PCR methods (Balinsky et al., 2008; Bowden et al., 2008) have been described. Although gel-based PCR is more time- and labour- consuming than real-time PCR, it is a cheap and reliable method, and is therefore useful in countries with limited resources. Recently, a real-time PCR method for simultaneous detection, quantitation, and differentiation of capripoxviruses was described by Lamien et al. (2011). The differentiation of lumpy skin disease virus from sheep pox and goat pox viruses is particularly important when characteristic clinical signs of capripox disease are detected in wild ruminants.
Lumpy skin disease virus cannot be distinguished serologically from sheep pox and goat pox viruses. Several methods have been used for serological investigations following outbreaks of LSD. A skin hypersensitivity test has been used successfully, for not all animals develop humoral antibody that can be detected by the available tests (Capstick and Coakley, 1962). Currently no sufficiently validated ELISA is commercially available for capripox diagnostics and therefore, virus-serum neutralisation tests are still considered as “gold standard” serological assays for capripoxviruses.
Various antibody ELISAs have been developed in the past with limited success. The earliest ELISA developed for capripoxviruses utilised a protein encoded by P32 (vaccinia H3L homoloque) as an antigen (Carn et al., 1994; Heine et al., 1999). More recently, an indirect ELISA was developed based on whole heat-inactivated sheep pox virus as an antigen (Babiuk et al., 2009). When 276 cattle serum samples were tested the diagnostic sensitivity and specificity of this assay were 88% and 97%, respectively. Unfortunately, due to difficulties in producing the inactivated antigen in sufficient quantities, this assay is currently not available for use in the open market. In another study, 42 open reading frames (ORF) of the capripoxvirus genome were evaluated for their antigenic potential and 2 ORFs encoding virion core proteins were selected as the best candidate antigens for use in ELISA. These proteins were then expressed in Escherichia coli and used as antigens for an indirect ELISA (Bowden et al., 2009). However, only 9 serum samples collected from 2 experimentally infected calves were available for evaluating the performance of the test. Recently, an ELISA based on a synthetic peptide targeting the major antigen P32 has been described for the detection of sheep pox and goat pox antibodies (Tian et al., 2010). Unfortunately the performance of this ELISA has not been evaluated using LSD cattle sera.
An indirect fluorescent antibody assay system has been widely used and gives antibody titres of up to 1/5000 in recovered animals. There are low titre cross relationships with cowpox virus in these tests but not with parapox group viruses (Weiss, 1968; Davies and Atema, 1981).
List of Symptoms/SignsTop of page
|Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate||Cattle & Buffaloes:All Stages||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Cattle & Buffaloes:All Stages||Diagnosis|
|Digestive Signs / Difficulty in prehending or chewing food||Cattle & Buffaloes:All Stages||Sign|
|Digestive Signs / Dysphagia, difficulty swallowing||Cattle & Buffaloes:All Stages||Sign|
|Digestive Signs / Esophageal obstruction||Cattle & Buffaloes:All Stages||Sign|
|Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism||Cattle & Buffaloes:All Stages||Sign|
|Digestive Signs / Melena or occult blood in faeces, stools||Cattle & Buffaloes:All Stages||Sign|
|Digestive Signs / Oral mucosal ulcers, vesicles, plaques, pustules, erosions, tears||Cattle & Buffaloes:All Stages||Diagnosis|
|Digestive Signs / Pharyngeal ulcers, vesicles, erosion, papules, sores pharynx||Cattle & Buffaloes:All Stages||Diagnosis|
|Digestive Signs / Tongue ulcers, vesicles, erosions, sores, blisters, cuts, tears||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Back swelling, mass back region||Sign|
|General Signs / Cyanosis, blue skin or membranes||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Cattle & Buffaloes:All Stages||Sign|
|General Signs / Forelimb lameness, stiffness, limping fore leg||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Generalized lameness or stiffness, limping||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass||Cattle & Buffaloes:All Stages||Sign|
|General Signs / Hindlimb lameness, stiffness, limping hind leg||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Cattle & Buffaloes:All Stages||Sign|
|General Signs / Lameness, stiffness, stilted gait in birds||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Laryngeal, tracheal, pharyngeal swelling, mass larynx, trachea, pharynx||Cattle & Buffaloes:All Stages||Sign|
|General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Mammary gland swelling, mass, hypertrophy udder, gynecomastia||Cattle & Buffaloes:Cow||Sign|
|General Signs / Neck swelling, mass cervical region||Cattle & Buffaloes:All Stages||Sign|
|General Signs / Oral cavity, tongue swelling, mass in mouth||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Pelvic or perineal swelling, mass||Sign|
|General Signs / Reluctant to move, refusal to move||Cattle & Buffaloes:All Stages||Sign|
|General Signs / Stiffness or extended neck||Cattle & Buffaloes:All Stages||Sign|
|General Signs / Swelling mass penis, prepuce, testes, scrotum||Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox||Sign|
|General Signs / Swelling mass, vulva, clitoris||Cattle & Buffaloes:Calf,Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow||Sign|
|General Signs / Swelling skin or subcutaneous, mass, lump, nodule||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Swelling, mass external abdomen||Cattle & Buffaloes:All Stages||Sign|
|General Signs / Swelling, mass tail||Sign|
|General Signs / Thoracic swelling, mass, thorax, chest, ribs, sternum||Sign|
|General Signs / Trembling, shivering, fasciculations, chilling||Cattle & Buffaloes:All Stages||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Weight loss||Cattle & Buffaloes:All Stages||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling||Sign|
|Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature||Cattle & Buffaloes:All Stages||Sign|
|Ophthalmology Signs / Conjunctival, scleral, redness||Cattle & Buffaloes:All Stages||Sign|
|Ophthalmology Signs / Corneal edema, opacity||Cattle & Buffaloes:All Stages||Sign|
|Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes||Cattle & Buffaloes:All Stages||Sign|
|Ophthalmology Signs / Purulent discharge from eye||Cattle & Buffaloes:All Stages||Sign|
|Pain / Discomfort Signs / Forelimb pain, front leg||Cattle & Buffaloes:All Stages||Sign|
|Pain / Discomfort Signs / Hindlimb pain, hind leg||Cattle & Buffaloes:All Stages||Sign|
|Pain / Discomfort Signs / Mouth, oral mucosal or tongue pain||Cattle & Buffaloes:All Stages||Sign|
|Pain / Discomfort Signs / Ocular pain, eye||Cattle & Buffaloes:All Stages||Sign|
|Pain / Discomfort Signs / Pain, penis||Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox||Sign|
|Pain / Discomfort Signs / Pain, pharynx, larynx, trachea||Cattle & Buffaloes:All Stages||Sign|
|Pain / Discomfort Signs / Pain, prepuce||Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox||Sign|
|Pain / Discomfort Signs / Skin pain||Cattle & Buffaloes:All Stages||Diagnosis|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Cattle & Buffaloes:Calf,Cattle & Buffaloes:Cow||Sign|
|Reproductive Signs / Agalactia, decreased, absent milk production||Cattle & Buffaloes:Cow||Diagnosis|
|Reproductive Signs / Anestrus, absence of reproductive cycle, no visible estrus||Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow||Sign|
|Reproductive Signs / Female infertility, repeat breeder||Cattle & Buffaloes:Cow||Diagnosis|
|Reproductive Signs / Male infertility||Cattle & Buffaloes:Bull||Diagnosis|
|Reproductive Signs / Mastitis, abnormal milk||Sign|
|Reproductive Signs / Papule, pustule, vesicle, ulcer penis or prepuce||Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox||Diagnosis|
|Reproductive Signs / Slough of mammary gland, udder||Sign|
|Reproductive Signs / Vaginal or cervical ulcers, vesicles, erosions, tears, papules, pustules||Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow||Sign|
|Reproductive Signs / Vulval ulcers, vesicles, erosions, tears, cuts, pustules, papules||Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow||Diagnosis|
|Respiratory Signs / Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring||Cattle & Buffaloes:All Stages||Diagnosis|
|Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs||Cattle & Buffaloes:All Stages||Sign|
|Respiratory Signs / Coughing, coughs||Cattle & Buffaloes:All Stages||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Cattle & Buffaloes:All Stages||Diagnosis|
|Respiratory Signs / Epistaxis, nosebleed, nasal haemorrhage, bleeding||Cattle & Buffaloes:All Stages||Diagnosis|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Cattle & Buffaloes:All Stages||Sign|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Cattle & Buffaloes:All Stages||Diagnosis|
|Respiratory Signs / Nasal mucosal ulcers, vesicles, erosions, cuts, tears, papules, pustules||Cattle & Buffaloes:All Stages||Diagnosis|
|Respiratory Signs / Purulent nasal discharge||Cattle & Buffaloes:All Stages||Diagnosis|
|Skin / Integumentary Signs / Moist skin, hair or feathers||Sign|
|Skin / Integumentary Signs / Purulent discharge skin||Cattle & Buffaloes:All Stages||Sign|
|Skin / Integumentary Signs / Rough hair coat, dull, standing on end||Cattle & Buffaloes:All Stages||Diagnosis|
|Skin / Integumentary Signs / Scarred skin||Cattle & Buffaloes:All Stages||Sign|
|Skin / Integumentary Signs / Skin crusts, scabs||Cattle & Buffaloes:All Stages||Diagnosis|
|Skin / Integumentary Signs / Skin edema||Cattle & Buffaloes:All Stages||Diagnosis|
|Skin / Integumentary Signs / Skin erythema, inflammation, redness||Cattle & Buffaloes:All Stages||Diagnosis|
|Skin / Integumentary Signs / Skin necrosis, sloughing, gangrene||Cattle & Buffaloes:All Stages||Diagnosis|
|Skin / Integumentary Signs / Skin papules||Cattle & Buffaloes:All Stages||Diagnosis|
|Skin / Integumentary Signs / Skin ulcer, erosion, excoriation||Cattle & Buffaloes:All Stages||Diagnosis|
Disease CourseTop of page
LSD in cattle
Animals of all age groups can become infected, and cases are common in young calves as well as all older age groups. The clinical picture of LSD in cattle follows an incubation period that varies from 4-12 days, and is usually about 7 days. There is a febrile reaction of 40-41.5°C, which may persist for 6-72 h or more rarely up to10 days. This is accompanied by lachrymation, increased nasal and pharyngeal secretions, anorexia, dysgalactia, general depression and a disinclination to move. There is great variation in the severity of these initial clinical signs, which do not relate to sex or age and they may be missed in extensively managed herds. Channel island breeds tend to more susceptible than others amongst Bos taurus types, and very severe cases are seen in many zebu breeds (MacDonald, 1931;von Backstrom,1945; Ayre-Smith, 1960).
Within 1-2 days, there is a sudden eruption of nodules in the skin of the animals, which may be widespread or restricted to just a few lesions. Predilection sites are the head and neck, the perineum, the genitalia, udder, and the limbs. Frequently the whole of the skin is covered with lesions. These are 5-50 mm in diameter, which are irregularly round, and appear as circumscribed areas of erect hair over a firm and slightly raised area of skin. This reaction is clearly separated from the adjacent healthy skin. There is hyperaemia in the affected areas and there may be beads of serum exuded from them. The lesions are of full skin thickness and involve epidermis, dermis and sub-cutis, often with some oedema. They slowly harden and form a dimple in the centre. The regional lymph nodes are enlarged to 3-5 times their normal size and are readily palpable. Some lumps may be detected in the subcutaneous tissues, which do not involve the skin. They are often distributed throughout the connective tissue and muscle in the body (Diesel, 1949). Lesions develop on the muzzle in the nares and the oropharynx. There is a typical ring-like lesion on the muzzle, as the necrotic lesion separates from the healthy surrounding epithelium. Lesions may also develop in the larynx and the trachea, throughout the alimentary tract but particularly in the abomasum. These nodules later become necrotic and ulcerate giving rise to severe gastro-enteritis. Muco-purulent discharges appear from the nares, persistent dribbling from the mouth, coughing and often stertorious and distressed respiration if the larynx and trachea are involved. Keratitis is a common complication.
The skin lesions gradually become harder and necrotic over a period of 2-3 weeks. Where hard oedematous plaques form in association with several lesions, they cause severe discomfort and pain and inhibit movement. In 2-3 weeks, they become harder and the core of necrotic tissue forms a plug, the "sitfast" of LSD. There is a discernable ring of live tissue around the lesions. The sitfast may slough away (but not all do so), leaving a full skin thickness hole in the skin, which heals by granulation. Bacteria may infect the hole. Inflammatory and oedematous swellings of the limbs may result in their being several times their normal size, large areas of necrotic lesions and hard skin over chronically oedematous limbs may slough away, leaving huge areas which can become infected or liable to myasis. This was a major concern when Cochliomyia homnivorax occurred in North Africa. Lesions on the teats may slough away, predisposing animals to mastitis and loss of quarters.
Pneumonia is a common sequel to LSD, which may be fatal. LSD lesions occur in the lungs as areas of grey consolidation measuring 20-30 mm. If these are widespread, interstitial pneumonia with consolidation and a fatal pneumonia may develop. Inhalation of necrotic tissue from lesions higher in the respiratory tract has been fatal many months after the initial infection. Abortion is common sequel of the acute phase of the disease; aborted foetuses and live calves have been observed with skin lesions of LSD. Infertility is a problem following LSD infection, females remain in anoestrous for several months and bulls, which suffer lesions on the genitalia, may be also infertile for months.
Extensive skin lesions and swollen limbs result in lameness and an inability to move. Mouth, pharyngeal, ocular and respiratory lesions prolong the period of anorexia and recovery. There is deterioration in the general condition of severely affected animals and under range conditions the mortality can be high. The recovery period is slow, and animals may be thin and weak for up to 6 months. The majority of affected animals develop comparatively few nodules and recover uneventfully. LSD is however, a serious disease affecting production, although the proportion of animals developing chronic complications may be low; less than 5% of those affected.
LSD in other hosts
Clinical LSD has not been observed in hosts other than cattle (Bos taurus and B. indicus), with the possible exception of the Asiatic water buffalo and the one case reported in an Arabian oryx. One million buffalo were exposed in Egypt in 1989, with no evidence of any clinical lesions. At times, there were many LSD cases in cattle sharing the same yards and premises as the buffalo. There was a report of LSD-like lesions in 5 buffalo in Egypt, which was not supported by virus isolation. Experimental inoculation of buffalo by the intra-dermal route did not produce LSD lesions. Recently, the persistence of LSDV nucleic acid was reported in skin samples collected from springbok (Antidorcas marsupialis) in South Africa (Lamien et al., 2011).
Experimental inoculation of giraffe, gazelle and impala (vide supra) resulted in the production of Capripox-like skin lesions, but no naturally infected animals have been observed in the field. Several species of wild ruminants do have antibody to Capripox virus in their sera however, suggesting that sub-clinical infection do occur (Hamblin et al., 1990). African buffalo sera collected in areas where LSD had occurred, had specific antibody to LSD (Davies, 1982).
The virus does not produce lesions in the skin of laboratory rabbits or rodents, but can be adapted by serial passage to grow on the chorio-allantoic membrane of embryonated eggs at 33.5-35°C. Camels (Camelus dromedarius) are not affected by LSD either naturally or by inoculation.
EpidemiologyTop of page
The disease occurs across the wide range of biotopes in Africa. It is seen in the wet coastal and central African tropical zones wherever cattle are kept, in the guinean and sudano-guinean zones in West Africa and the wetter bushed and wooded grasslands in the drier Acacia type grasslands that are found throughout the continent, and in the semi-arid and arid zones. LSD occurs in the higher altitude temperate-type grasslands on plateaux up to an altitude of 7500-8000 ft. The successful transmission of LSD in all these diverse habitats suggests that there must be variety of arthropod vectors capable of transmitting the virus. Low lying wet areas with abundant vector populations are those which suffer from greater morbidity in cattle. For example, irrigated areas of Egypt in the delta, oases and along the Nile provided ideal conditions for LSD transmission in the summer months when mosquito populations are extremely high.
Source of virus
Latency or intermittent secretion of virus does not occur with LSD. At the acute stage of the disease the nasal, lachrymal and pharyngeal secretions contain virus for 10-12 days and there may be contagion from such sources early in the course of the disease. Beads of infected serum appear on early skin lesions, which are infective and attract flies. Contagion does not occur readily with LSD, but can happen rarely if animals share water troughs. The duration of viraemia usually varies between 1 to 12 days. Viral DNA may be detected in blood samples using PCR method up to 17 days and in infected skin lesions for 4-6 months or longer. Poxviruses are extremely resistant to desiccation in tissue, and animals have been seen with LSD necrotic skin lesions in-situ 2 years after infection. A more recent study demonstrated the persistence of live virus in bovine semen for up to 42 dpi and viral DNA was detected until 159 dpi (Irons et al., 2005).
The movement of animals from infected herds, often months after recovery, has regularly resulted in the introduction of infection. The source of the virus is considered to be from old skin lesions. In most of Sub Saharan Africa, the disease has been observed to appear following the seasonal rains, when there is always an increase in the population of different arthropod species. Local movement of the disease in the presence of strict quarantines has been attributed to aerial movement of insect vectors in low-level air currents. The onset of frosts in South Africa and Egypt results in a great fall in the number of cases of LSD, which virtually disappears over the winter to reappear again in the spring and summer. The disease spread throughout Egypt in the summer of 1989, despite total restrictions of animal movements. A focus of LSD appeared in Israel some 80-200 km distant from active foci of LSD transmission in Egypt, this suggests that aerial movement of biting insects had occurred. The imposition of quarantines does prevent the spread of infection by recovered animals but not by the aerial movement of vectors.
Direct contact is considered to be an ineffective means of transmission. Communal cattle grazing and watering points have been associated with the occurrence of LSD. Transmission of LSDV through semen (natural mating or artificial insemination) has not been experimentally demonstrated, but LSDV has been isolated in the semen of experimentally infected bulls (Weiss, 1968; Irons et al., 2005).
The transmission of LSD by insects is thought to be mechanical, as it is with fowl pox; there is a wide range of biting flies with the potential to transmit virus. High morbidities are seen where mosquito populations are abundant, with 50-60% attack rates; and low, 5-15% morbidity in arid environments where there are fewer potential mechanical vectors.
Any biting fly could theoretically transmit a poxvirus after an interrupted feed on a viraemic host. The virus has been recovered from Stomoxys and Biomyia spp. in South Africa, and Stomoxys have been shown to be capable of transmitting Capripox viruses. Mosquitoes have been found feeding upon cattle in huge numbers in epizootics and are capable of transmitting many viruses by mechanical means (Chihota et al., 2001). Tabanids, Culicoides and Glossina spp. may all have the potential to transmit LSD, as all feed voraciously upon domestic cattle (Weiss, 1968; Kitching and Mellor, 1986; Carn and Kitching, 1995).
Recently, new evidence has been published reporting a possible role for hard ticks in the transmission of LSDV (Tuppurainen et al., 2011). The study showed molecular evidence of transstadial and transovarial transmission of LSDV by Rhipicephalus (Boophilus) decoloratus ticks, and mechanical or intrastadial transmission by Rhipicephalus appendiculatus and Amblyomma hebraeum ticks.
Inter-seasonal or inter-epizootic maintenance
In favourable wet years, the epizootic spread of LSD can occur on a countrywide basis. High morbidity rates may be seen, and then after a lower level of transmission during the dry seasons, more extensive transmission resumes again after the seasonal rains. This cycle may persist for 1-3 years before the disease disappears.
For several years no LSD may be seen, although occasional foci affecting 1-2 herds may appear. These have been investigated and have often been in isolated situations where the only possible indirect contact with other bovids, has been with buffalo (Syncerus caffer). These populations were investigated and shown to have Capripox antibody. The identification of any inter-epizootic maintenance system has proved to be difficult. Lesions on recovered cattle are probably the principle source of virus for long interval transmission cycles. These are clearly the source in many outbreak situations and where the disease has been introduced into another country. There is a possibility that other ruminant species may be involved in this cycle and buffalo and some other game species are likely candidates. There has been no evidence for a change in the level of host affinity, where LSD arises from Capripox-infected sheep or goats. This was initially suspected in one outbreak in Kenya, but no further evidence has accrued to show that this happens.
Risk factors and predictive epidemiology
LSD is one of a group of African viral diseases that are known to be precipitated by the periodic cycles of rainfall, which are determined by the characteristics of the inter tropical convergence zone (Davies et al., 1986). The relationship of epizootic activity to this has been studied with regard to Rift Valley and ephemeral fever, but not yet with LSD (Davies, 1990). However, the periods of widespread regional and national epizootics has been correlated with these periods of heavy rainfall in East and West Africa. Further studies are necessary to develop predictive tools for LSD and to drive strategic vaccination.
In general, the Bos taurus breeds imported into Africa to improve production potential tend to be more susceptible to LSD than indigenous Bos indicus breeds. The risks for breeds such as the Channel Island breeds (Jersey, Guernsey, etc) or Friesian/Holstein are greatest because they are usually kept in high production systems where the losses are likely to be more pronounced. The routine vaccination of such animals is a sensible precaution against losses.
Impact: EconomicTop of page
The occurrence of LSD in West Africa in 1997-8 caused serious problems, particularly in the guinean and sudano-guinean zones. The disease appeared after the onset of the rains at a time when draught oxen were required for cultivation and the planting of crops by subsistence farmers. The onset of disease in oxen at this time resulted in a failure to cultivate and plant crops. This constituted a serious hazard to the food security of the people in the affected areas and produced an overwhelming response for vaccine.
The first countrywide South African epidemic of LSD affected some 8 million cattle. On some farms, the morbidity approached 100% and was regularly between 50-100%. The mortality rates were normally low (1-5%; about standard for the disease), but were occasionally reported to be much higher (Diesel, 1949), with significant amounts of hide damage occurring. Losses to the Egyptian hide industry after their first epidemic were high; income fell by a half. Loss in production, either in terms of beef or milk, for severely affected animals may be considerable, with severely affected animals suffering debility for 2-6 months, dependent on the severity of lesions (Diesel, 1949). Vaccination costs constitute an important cost during epidemics, and normally to provide routine protection against disease. Costs are recurrent and include the cost of the vaccine, refrigerated transportation, needles, syringes and costs of employing veterinarians. The costs of dealing with the initial focus of LSD in Israel were US$ 750,000.
There is potential for further geographic spread of LSD, and there is a real need for increased surveillance in countries adjacent to those already infected and along trade routes in affected regions (Davies, 1991).
Zoonoses and Food SafetyTop of page
LSD poses no zoonotic problems. Infected cattle are a not a source of any infection for humans and milk is safe to enter the human food chain. Whilst it is not desirable to eat the flesh of infected animals, due to the likelihood of carcass contamination by secondary bacterial infections, no harm has been known to have resulted from its consumption.
Disease TreatmentTop of page
There is no effective treatment for LSD. Supportive antibiotic and anti-inflammatory painkiller therapy is used, whenever pyaemic changes or cellulitis occur in association with lesions. Water should be provided for animals unable to move and the secondary mastitis arising from teat or udder lesions requires antibiotic infusions or injections.
Prevention and ControlTop of page
LSD has frequently been introduced into a previously unaffected area or country by the movement of live animals from a region or a country where LSD virus activity has occurred. A clinical examination of these animals may have been carried out, and they may have been in good health with no obvious signs of disease. To detect cattle with just a few lesions would require careful examination by a trained investigator, and missing recovered cases is all that would be required to allow the disease to be introduced. The level of disease surveillance, which is necessary to detect low levels of LSD virus activity is not widely available in many of the sub-Saharan countries, where animal health services operate with low budgets; active surveillance activities cannot be funded.
The risk of LSD arising from local or regional movement of cattle is therefore high. Quarantine facilities in importing countries, where cattle can be held for inspection, are generally inadequate to control insect-borne diseases. Insect-proofed quarantine facilities are rare, and transmission can occur from the open yards where cattle are usually held or in transit from a ship or lorry.
Serological tests may have a role to play in regularising trade from infected areas. At present the tests, when they are available, do not detect all recent cases of disease. Some animals do not appear to develop a humoral antibody response to infection, and this proportion is thought to be of the order of 10%. The intra-dermal sensitivity test is cheap and detects a cellular level response to LSD virus. It may have a role to play in screening animals for export, if further evaluation studies are made. PCR methods can be used to detect viraemic animals with or without clinical disease.
Introduction of LSD by insect vectors
Field observations show that with the imposition of quarantine regulations, extension of LSD from known foci of disease still occurs on a local or sub-regional basis. Local air currents can allow this to happen, whereby insects are carried on the prevailing winds. This was the likely means by which LSD virus moved to create a new focus of infection in Israel from the known sites of virus activity in Egypt some 80-200 km to the west. Such introductions could in the future occur into a number of receptive areas in the near and Middle East from foci of activity in Arabia or Egypt. Emergency preparedness for an outbreak of LSD should be made in those countries at risk.
There is much evidence to show that air currents can carry pathogen-laden insect pests over long distances. Locusts and many plant pests for example are known to appear in continents far distant from Africa. An incident has occurred whereby Anopheles pharoensis was carried by air currents from the Nile delta in Egypt, to establish a focus of malarial transmission near Haifa in Israel (Garret Jones, 1962).
Immunization and Vaccines
Only live attenuated vaccines against LSD are currently commercially available. Due to antigenic homology and cross protection between sheep pox, goat pox and LSD viruses, any of these viruses can be used as a vaccine strain to protect cattle against LSD.
Two vaccines have been widely used against LSD. One was developed in South Africa from a modified live virus strain of LSD, which had been passaged in lamb kidney cells (60 times) and embryonated eggs (20 times). This vaccine is produced in tissue cultures and is immunogenic (Weiss, 1968). It has the disadvantage that it produces a granulomatous reaction in up to half of the vaccinated animals, which results in some owner resistance to its use. A vaccine strain was developed in Kenya from a strain of sheep pox originating in the Kedong Valley, which had been passaged 16 times in lamb testis cells. A complete cross immunity had been demonstrated to exist between strains of sheep pox and LSD. This strain was used for many years at an immunising dose of 10 3.5 TCID 50 (Capstick and Coakley, 1961, 1962). Local reactions also occurred with this vaccine, but in a much lower proportion of cases (9.6%). No generalisation of lesions has ever been detected following its use, and for this reason it has been the vaccine strain of choice in East Africa for many years. No cases of sheep or goat pox were found to be associated with its use over a period of 25 years or more (Capstick and Coakley, 1961).
A Capripox vaccine strain was developed in Kenya from a sheep and goat pox isolate (O/240), which was modified for virulence by passage in a foetal muscle cell line. This modification occurred at the 15th passage and the vaccine was used in small ruminants at the 17-20th passage levels (Davies and Mbugwa, 1985). It had an ID50 of 5 TCID 50 and was thus a potent immunogen. In emergency situations this vaccine has also been used for LSD vaccination, and it proved to be safe and potent in Bos indicus breeds but caused mild generalised lesions in a proportion of Bos taurus breeds. The complication rate overall was low (0.2-2%) but was occasionally higher in individual herds of susceptible breeds. The generalisation has not be reproduced in susceptible breeds at the laboratory, with 1000 times the virus challenge, although regional lymph node enlargement has been seen.
In Egypt, a Romanian strain of sheep pox was used in cattle during the epidemic. This was produced by the classic Borrel method from infected fluids in lambs. It proved to be protective against the rapid epizootic spread of LSD. A tissue culture-adapted Romanian sheep pox strain was used on a limited basis in Israel, and it was found that a 10 times higher immunising dose was required, compared with that recommended for sheep (Michael et al., 1997). A recombinant Capripox vaccine is being developed and the initial results are promising (Romero et al., 1994).
During recent LSD outbreaks in the Middle East region it was reported that vaccination did not result in a complete protection against the disease in each vaccinated animal (Brenner et al., 2009). However, vaccination is currently the only effective way to control the spread of LSDV in endemic countries. In non-endemic areas the use of live attenuated vaccines may compromise the disease-free status of the country and would be highly questionable on grounds of safety. In addition, the use of genetically modified recombinant live vaccines may not be permitted. In non-endemic countries the use of inactivated vaccines could be considered as a short term solution in an emergency; however the protection provided by inactivated vaccines is not solid and is only short-lived.
The eradication of LSD has not proved possible in any of the African countries where it has occurred. Control has been achieved by a combination of quarantine and ring vaccination policies. The incidence of disease has been greatly reduced in Egypt by annual vaccination to the point where only one or two outbreaks now occur annually. LSD appears to be extremely difficult to eradicate once it has become enzootic amongst a cattle population.
ReferencesTop of page
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